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Pancreatic Neoplasms: HELP
Articles by F. Wang
Based on 11 articles published since 2010
(Why 11 articles?)

Between 2010 and 2020, F. Wang wrote the following 11 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article [Clinicopathological features and prognosis of 488 patients with neuroendocrine tumors]. 2019

Zhai, X J / Yu, S L / Ma, Y H / Wang, F / Yang, M J / Lian, Y J / Yu, X X / Fan, Q X / Song, L J. ·Department of Oncology, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. · Department of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. · Department of Pathology, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. ·Zhonghua Yi Xue Za Zhi · Pubmed #31484281.


2 Article Differential MicroRNA Expression Profiles as Potential Biomarkers for Pancreatic Ductal Adenocarcinoma. 2019

Zhu, Y / Wang, J / Wang, F / Yan, Z / Liu, G / Ma, Y / Zhu, W / Li, Y / Xie, L / Bazhin, A V / Guo, X. ·Department of Oncology, International Joint Laboratory for Cell Medical Engineering of Henan Province, Henan University Huaihe Hospital, Kaifeng, Henan, 475000, P. R. China. celltransplant@163.com. · Department of Oncology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450014, P. R. China. wj68happy@hotmail.com. · Department of Preventive Medicine, Cell Signal Transduction Laboratory, Joint National Laboratory for Antibody Drug Engineering, Institute of Biomedical Informatics, Medical School, Henan University, Kaifeng, Henan, 475004, P. R. China. · Department of Oncology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450014, P. R. China. · College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, Tianjin, 300353, P. R. China. mayonggang@nankai.edu.cn. · Department of Anesthesia, Stanford University, CA 94305, USA. wan.zhu@stanford.edu. · Department of General, Visceral, and Transplantation Surgery, Ludwig-Maximilians-University Munich, Munich, 81377, Germany. alexandr.bazhin@med.uni-muenchen.de. · Department of Preventive Medicine, Cell Signal Transduction Laboratory, Joint National Laboratory for Antibody Drug Engineering, Institute of Biomedical Informatics, Medical School, Henan University, Kaifeng, Henan, 475004, P. R. China. xqguo@henu.edu.cn. ·Biochemistry (Mosc) · Pubmed #31234772.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) remains a clinical challenge due to its poor prognosis. Therefore, the early diagnosis of PDAC is extremely important for achieving a cure. MicroRNAs (miRNAs) could serve as a potential biomarker for the early detection and prognosis of PDAC. In this work we analyzed plasma samples from healthy persons and PDAC patients to assess differential miRNA expression profiles by next generation sequencing technology and bioinformatics analysis. In this way, 165 mature miRNAs were found to be significantly deregulated in the patient group, of which 75 and 90 mature miRNAs were up- and down-regulated compared with healthy individuals, respectively. Furthermore, 1029 novel miRNAs were identified. In conclusion, plasma miRNA expression profiles are different between healthy individuals and patients with PDAC. These data provide a possibility for use of miRNA as diagnostic and prognostic biomarkers of PDAC.

3 Article ["Liver and pancreas oriented" strategies for minimally invasive surgery of biliary malignant tumors]. 2019

Liu, R / Wang, F. ·Second Department of Hepatobiliary Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China. ·Zhonghua Wai Ke Za Zhi · Pubmed #30612388.

ABSTRACT: Surgery of biliary malignant tumors is highly related to the liver and pancreas. The "Liver and pancreas oriented" characteristics are unavoidable challenges when formulating surgical strategies. In the development of minimally invasive surgery for biliary malignant tumors, a comprehensive understanding of the pattern of the biliary surgery can make innovation possible. Both the bleeding prevention in hepatectomy and the exposure in pancreatic surgery are the core of minimally invasive surgery for biliary malignant tumors. The relationships between the minimally invasive surgery and the open surgery, laparoscopic and robotic surgery, the biliary tumors and adjacent liver and pancreas are essential to the surgical the progress of the minimally invasive biliary surgery.

4 Article Adverse tumor biology associated with mesenterico-portal vein resection influences survival in patients with pancreatic ductal adenocarcinoma. 2014

Wang, F / Gill, A J / Neale, M / Puttaswamy, V / Gananadha, S / Pavlakis, N / Clarke, S / Hugh, T J / Samra, J S. ·Department of Gastrointestinal Surgery, Royal North Shore Hospital and North Shore Private Hospital, University of Sydney, St Leonards, NSW, Australia, fwang1881@gmail.com. ·Ann Surg Oncol · Pubmed #24558067.

ABSTRACT: BACKGROUND: Although pancreatoduodenectomy (PD) with mesenterico-portal vein resection (VR) can be performed safely in patients with resectable pancreatic ductal adenocarcinoma (PDAC), the impact of this approach on long-term survival is controversial. PATIENTS AND METHODS: Analyses of a prospectively collected database revealed 122 consecutive patients with PDAC who underwent PD with (PD+VR) or without (PD-VR) VR between January 2004 and May 2012. Clinical data, operative results, and survival outcomes were analysed. RESULTS: Sixty-four (53 %) patients underwent PD+VR. The majority (84 %) of the venous reconstructions were performed with a primary end-to-end anastomosis. Demographic and postoperative outcomes were similar between the two groups. American Society of Anesthesiologists (ASA) score, duration of operation, intraoperative blood loss, and blood transfusion requirement were significantly greater in the PD+VR group compared with the PD-VR group. Furthermore, the tumor size was larger, and the rates of periuncinate neural invasion and positive resection margin were higher in the PD+VR group compared with the PD-VR group. Histological venous involvement occurred in 47 of 62 (76 %) patients in the PD+VR group. At a median follow-up of 29 months, the median overall survival (OS) was 18 months for the PD+VR group, and 31 months for the PD-VR group (p = 0.016). ASA score, lymph node metastasis, neurovascular invasion, and tumor differentiation were predictive of survival. The need for VR in itself was not prognostic of survival. CONCLUSIONS: PD with VR has similar morbidity but worse OS compared with a PD-VR. Although VR is not predictive of survival, tumors requiring a PD+VR have more adverse biological features.

5 Article The clinical impact of early complete pancreatic head devascularisation during pancreatoduodenectomy. 2013

Gundara, J S / Wang, F / Alvarado-Bachmann, R / Williams, N / Choi, J / Gananadha, S / Gill, A J / Hugh, T J / Samra, J S. ·Upper Gastrointestinal Surgical Unit, Royal North Shore Hospital, University of Sydney, St Leonards, Australia. ·Am J Surg · Pubmed #23809671.

ABSTRACT: BACKGROUND: Early inferior pancreaticoduodenal artery (IPDA) ligation reduces intraoperative blood loss during pancreatoduodenectomy, but the impact on oncologic and long-term outcomes remains unknown. The aim of this study was to review the impact of complete pancreatic head devascularization during pancreatoduodenectomy on blood loss, transfusion rates, and clinicopathologic outcomes. METHODS: Clinicopathologic and outcome data were retrieved from a prospective database for all pancreatoduodenectomies performed from April 2004 to November 2010 and compared between early (IPDA+; n = 62) and late (IPDA-; n = 65) IPDA ligation groups. RESULTS: Early IPDA ligation was associated with reduced blood loss (394 ± 21 vs 679 ± 24 ml, P < .001) and perioperative transfusion (P = .031). A trend toward improved R0 resection was seen in patients with pancreatic adenocarcinoma (IPDA+ vs IPDA-, 100% vs 82%; P = .059), but this did not translate to improved 2-year (IPDA+ vs IPDA-, 76% vs 65%; P = .426) or overall (P = .82) survival. CONCLUSIONS: Early IPDA ligation reduces blood loss and transfusion requirements. Despite overall survival being unchanged, a trend toward improved R0 resection is encouraging and justifies further studies to ascertain the true oncologic significance of this technique.

6 Article β2-AR-HIF-1α: a novel regulatory axis for stress-induced pancreatic tumor growth and angiogenesis. 2013

Shan, T / Ma, J / Ma, Q / Guo, K / Guo, J / Li, X / Li, W / Liu, J / Huang, C / Wang, F / Wu, E. ·Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China. ·Curr Mol Med · Pubmed #23745588.

ABSTRACT: The purpose of this study was to test the hypothesis that chronic stress in a negative social and psychological state plays a critical role in pancreatic cancer development and progression. In this study, we created a new stress model system to determine the effects of chronic stress on pancreatic cancer progression. Here, we show that chronic stress not only causes depression in mice, most likely attributed to an elevated level of epinephrine, but also induces pancreatic cancer progression. We provide evidence that the pancreatic cancer progression induced by chronic stress could be blocked to a significant degree by β2-AR inhibitor ICI118 551 or HIF-1α inhibitor 2-methoxyestradiol. Moreover, establishment of pancreatic cancer in mice exposed to chronic stress was accompanied by up-regulation of the expression of MMP-2, MMP-9, and VEGF, mediated by a HIF- 1α-dependent β-AR signaling pathway. Our data suggest that the β2-AR-HIF-1α axis regulates stress-induced pancreatic tumor growth and angiogenesis. This study may have a therapeutic or preventive potential for the patients with pancreatic cancer who are especially prone to psychosocial stress challenges.

7 Article Pancreatic cancer cells expressing hypoxia-inducible factor-1α tend to be adjacent to intratumoral blood vessels. 2010

Cheng, B-Q / Segersvärd, R / Permert, J / Wang, F. ·Department of Surgery, Karolinska University Hospital, Huddinge, Sweden. ·Eur Surg Res · Pubmed #20924188.

ABSTRACT: We investigated whether cells expressing hypoxia-inducible factor-1α (HIF-1α) are specially related to blood vessels in human pancreatic tumors. HIF-1α and blood vessels were stained in 7 pancreatic ductal adenocarcinomas (PDAC) and 3 nonmalignant tumors. HIF-1α(+) cells accounted for 37 ± 5% of the total PDAC cells and increased to 52 ± 4% in perivascular PDAC cells and to 67 ± 4% in PDAC cells found in intratumoral blood vessels. In nonmalignant tumors, 12 ± 3% of the total tumoral cells examined were HIF-1α(+), and HIF-1α(+) cells decreased to 2 ± 0.3% in perivascular cells examined in the tumors. In conclusion, HIF-1α(+) cells in PDAC and nonmalignant pancreatic tumors differ not only in their amounts but also in their relation to intratumoral blood vessels. HIF-1α(+) cells usually are adjacent to intratumoral blood vessels in PDAC tumors, but are farther away from the vessels in nonmalignant pancreatic tumors.

8 Article hsa-miR-520h downregulates ABCG2 in pancreatic cancer cells to inhibit migration, invasion, and side populations. 2010

Wang, F / Xue, X / Wei, J / An, Y / Yao, J / Cai, H / Wu, J / Dai, C / Qian, Z / Xu, Z / Miao, Y. ·Laboratory of General Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, PR China. ·Br J Cancer · Pubmed #20628378.

ABSTRACT: BACKGROUND: Expression of ABCG2 is normally absent or low in the pancreas, but high in human pancreatic cancer cells. The mechanism by which ABCG2 is altered in human cancers remains unknown. METHODS: We investigated ABCG2 expression in four pancreatic cancer cell lines, and used three microRNA (miRNA) target prediction programmes, and information from the existing literature to predict and identify hsa-miR-520h as an miRNA that targets ABCG2. The function of this miRNA was investigated by transient transfection of the pancreatic cancer cell line PANC-1 with oligonucleotides that mimic hsa-miR-520h. RESULTS: Results showed that both mRNA and protein levels of ABCG2 were reduced, indicating that it was a target of hsa-miR-520h. Introduction of hsa-miR-520h mimics into PANC-1 cells also resulted in inhibition of cell migration and invasion, and reduction of side population cells. Cell proliferation, cell cycle progression and apoptosis were not affected. CONCLUSIONS: We propose that the effects of hsa-miR-520h may be, at least in part, caused by its regulation of ABCG2. Thus, our findings provide a new insight into the function of miRNA in the regulation of ABCG2 expression in pancreatic cancer. Gene therapy using miRNA mimics may therefore be useful as a pancreatic cancer therapy.

9 Article Activation of EGFR by proteasome inhibition requires HB-EGF in pancreatic cancer cells. 2010

Sloss, C M / Wang, F / Palladino, M A / Cusack, J C. ·Department of Surgery, Division of Surgical Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ·Oncogene · Pubmed #20208558.

ABSTRACT: Resistance to drug treatments underlies the high lethality of pancreatic ductal adenocarcinoma. Along with others, we have recently identified that proteasome inhibition is a promising therapeutic option in this highly refractory disease. The pleiotropic effects of proteasome inhibition include the activation of apoptotic signaling pathways and also antiapoptotic signaling pathways such as EGFR, AKT and the MAP kinases that reduce the apoptotic potential of this class of drug. In this study, we sought to determine the mechanism behind the activation of EGFR in response to proteasome inhibition in pancreatic cancer cells. We found that the second-generation proteasome inhibitor NPI-0052 induced the mRNA transcription of several EGFR family ligands (EGF, HB-EGF and epiregulin), however only increases in HB-EGF were detected at the protein level. Using both pharmacological inhibitors and lentiviral-mediated shRNA knockdown of EGFR ligand expression, we discovered that ligand cleavage by MMP/ADAMs and HB-EGF expression is required for activation of EGFR in response to proteasome inhibition. Furthermore, we discover that induction of HB-EGF is dependent on reactive oxygen species and p38-MAPK signaling but not ERK and that the transcription factor SP-1 is involved in NPI-0052-induced HB-EGF transcription. Together, these results indicate that stress signaling leading to induction of HB-EGF expression and increases in MMP/ADAM-dependent HB-EGF cleavage are responsible for proteasome inhibitor-induced activation of EGFR in pancreatic cancer cells.

10 Article Suppression effects of AICAR on insulin secretion involved in peroxisome proliferator-activated receptor gamma changes in INS-1 cells. 2010

Guo, H / Zhang, X J / Wang, F / Wang, Y / Shen, Y / Zhao, J J / Gao, L. ·Central Laboratory, Provincial Hospital affiliated to Shandong University, No. 324, Jing 5 Road, Jinan, 250021, China. gaoling1@medmail.com.cn ·J Endocrinol Invest · Pubmed #20101096.

ABSTRACT: BACKGROUND: AMP-activated protein kinase (AMPK) activation is known to attenuate glucose-stimulated insulin secretion (GSIS) in pancreatic beta cells. However, the underlying mechanisms are poorly understood. The purpose of this study was to examine the effects of AMPK activation on insulin secretion and to determine whether peroxisome proliferator-activated receptors (PPAR) are involved in the effects on INS-1 cells. METHODS: INS-1 cells, insulinoma cell lines, were treated with an activator (AICAR) or inhibitor (Compound C) of AMPK as well as inhibitors of PPAR [MK886 and biphenol A diglycidyl ether (BADGE)] for different treatment times. RESULTS: AICAR-induced AMPK activation significantly attenuated GSIS as well as insulin content. Meanwhile, AMPK activation increased the mRNA levels of both PPARalpha and PPARgamma. However, with regard to DNA binding, AMPK activation upregulated PPARgamma only, and it was possible to reduce the increment with the AMPK inhibitor. Moreover, the AICAR-induced suppression of insulin secretion can be counteracted by the PPARgamma inhibitor, BADGE but not the PPARalpha inhibitor. CONCLUSIONS: AICAR-induced glucose-stimulated insulin secretion reduction correlates mainly with PPARgamma changes.

11 Retraction MicroRNA-215 functions as a tumor suppressor and directly targets ZEB2 in human pancreatic cancer. 2015

Li, Q W / Zhou, T / Wang, F / Jiang, M / Liu, C B / Zhang, K R / Zhou, Q / Tian, Z / Hu, K W. ·Department of Oncology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China. ·Genet Mol Res · Pubmed #26662405.

ABSTRACT: It has been shown that microRNA-215 (miR-215) is dysregulated in several human malignancies, and this correlates with tumor progression. However, its expression and function in pancreatic cancer is still unclear. The aim of this study was to explore the effects of miR-215 on pancreatic cancer formation and progression. Using quantitative RT-PCR, we detected miR-215 expression in pancreatic cancer cell lines and primary tumor tissues. The association of miR-215 expression with clinicopathological factors and prognosis was also analyzed. We then observed the effects of miR-215 on the biological behavior of pancreatic cancer cells. Lastly, the potential regulatory function of miR-215 on ZEB2 expression was investigated. miR-215 expression levels were significantly downregulated in pancreatic cancer samples and cell lines. Decreased miR-215 expression was significantly associated with large tumor size, advanced TNM stage, lymph node metastasis, vessel invasion, and lower overall survival. Multivariate regression analysis corroborated that downregulation of miR-215 was an independent unfavorable prognostic factor. Overexpression of miR-215 inhibited pancreatic cancer cell proliferation, invasion, and migration; promoted cell apoptosis in vitro; and suppressed tumorigenicity in vivo. Further, ZEB2 was confirmed as a direct target of miR-215 by using a luciferase reporter assay. These findings indicate that miR-215 may act as a tumor suppressor in pancreatic cancer cells, and could serve as a novel therapeutic target for miR-based therapy.